Autism is a disorder of social, intellectual and language functioning. Until recently, few clues to the anatomical basis of autism existed. In 1985, we proposed that a highly probable site of pathology in autism is the neocerebellum. We then tested and confirmed this hypothesis by showing with magnetic resonance (MR) technology that the neocerebellar vermis in autism was statistically significantly reduced in size in 30 adolescents and adults with autism relative to 30 normal controls. We also reported that the cerebellar hemispheres are significantly smaller in autistic subjects. Based on the site and the morphology of the vermian abnormalities, we proposed that these abnormalities are due to early developmental damage that could mark the onset of autism. We now propose to study neuroanatomical development in autism in far greater detail; our findings may have a major impact on the understanding of the etiology, neuroanatomy and neurophysiology of autism. The following issues will be addressed: 1. Are cerebellar abnormalities present at the time of the appearance of the earliest detectable behavioral symptoms of autism (age 2-4 years)? 2. If the cerebellar abnormalities have an early onset, do these abnormalities change with age, or do they remain stable throughout development? 3. If cerebellar abnormalities have a late onset, what is the developmental time-course of these abnormalities? 4. Are there abnormalities of other brain structures present in autism? I so, what are the onset times and developmental time-course of damage within these structures? The structures of greatest interest are: the frontal, temporal, parietal and occipital lobes; the hippocampus; he ventricular system; the basal ganglia; the corpus callosum; the thalamus; and the brainstem. Using MR, we propose to measure the cerebellum and additional CNS structures of greatest interest in groups of retarded and non-retarded autistic children and adolescents of ages 2-4, 6-7, 10-11 and 14-16 years. We will measure the same structures in non-sedated, normal volunteers of comparable age; in-depth comparisons will be performed; longitudinal data will be obtained by re-imaging the three younger groups of autistic abnormal subjects at a later age. Age-related effects will be analyzed.